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Anti-inflammatories: brain on fire


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Soothe the brain on fire...
 
Anti-inflammatories will not cure HPPD but might provide a useful adjunct to treatment. Soothing neuroinflammation might even be a required part of healing. I've copied and pasted relevant information, with sources below. Please add information.
 
Key concepts related to brain inflammation:
 
• Your brain is saturated with immune cells called microglia cells.
 

• The microglia cells perform many important functions under normal conditions to help transmission between neurons, such as removal of dead neurons and plaques.
 
• In a heightened state of activation, microglia create a persistent, self-perpetuating state of neuroinflammation.
 
• Microglia cells can become activated and promote neuroinflammation in response to inflammatory diets, head trauma, lack of oxygen, diabetes, environmental toxins, autoimmunity, and systemic inflammation.
 
• Neuroinflammation decreases the speed of neuron responses and leads to symptoms such as brain fog and depression. Chronic neuroinflammation leads to neuron death and neurodegenerative changes.
 
[Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? ]

 

Inflammation is a lifesaving process used by the immune system to combat infection. But sometimes the inflammatory response is inappropriately activated. The most blatant examples are autoimmune disorders, in which the immune system ignites a full-fledged attack against the body’s own tissues,making natural anti-inflammatories necessary.
However, chronic low-level inflammation also takes its toll. It releases compounds that are toxic to neurons and unleashes a cascade of free radicals that damage and destroy brain cells.
Brain tissues affected by Alzheimer’s are rife with inflammatory chemicals. In addition, blood levels of C-reactive protein (CRP), a marker of inflammation, are linked with increased risk of the disease. Therefore, addressing inflammation with natural anti-inflammatories is critical for protecting against Alzheimer’s and its progression.

 
 
Summary of potentially useful agents:

  • Fish Oil/DHA
  • Apigenin
  • Baicalein
  • Resveratrol
  • Rutin
  • Catechins
  • Curcumin
  • Aspirin
  • Estrogens
  • N-acetylcysteine (NAC)
  • Astaxanthin

Tips:

  • Go easy on meat and egg yolks, which contain pro-inflammatory arachidonic fatty acids, and eat more fish—nature’s best source of anti-inflammatory omega-3 fats. Studies show that people who eat fish just once a week reduce their risk of Alzheimer’s by 60 percent.
  • In addition to eating fish, recommend taking 2–4 grams of high-quality fish oil daily. Low levels of the omega-3 fat DHA have been linked with Alzheimer’s as well as other types of dementia and mood disorders.

One of the most abundant fats in the brain, DHA helps construct robust cellular membranes and protective myelin sheaths. It also turns on genes for brain-derived neurotrophic factor (BDNF), which makes neurons more resistant to injury and free-radical damage.
[The Alzheimer’s Disease Neuroimaging Initiative (ADNI), a large, multicenter study funded by the National Institutes of Health, also found that long-term use of fish oil supplements was associated with reduced age-related shrinkage of the brain and better cognitive function in older adults identified as having “normal cognition” at the start of the three year study.
 
http://www.drwhitaker.com/protect-your-brain-with-natural-anti-inflammatories]
 
 
Apigenin (flavonoid)
Apigenin is a bioflavonoid found in parsley, artichoke, basil, and celery. It has very powerful neuroinflammation quenching and neuroprotective properties. Research has demonstrated the compound can modulate activation of the microglia cells during neuroinflammatory processes. Apigenin has demonstrated the ability to inhibit microglial proliferation. Apigenin has also demonstrated the ability to protect neuronal cells from artery occlusion that may occur after stroke. 50 51 52 53 Luteolin Luteolin is a bioflavonoid found in celery and green peppers and has been shown to block inflammatory responses in the brain by inhibiting microglia activation. Luteolin has been shown to inhibit several different microglial activating pathways and demonstrated the ability to protect neurons from inflammation-induced injury in research studies. 54 55 56 57
 
Baicalein (flavonoid)
Baicalein is a flavonoid that has been shown to exert anti-inflammatory and antioxidant properties on the brain microglia system. 58 It has a long history of safe administration to humans and has been found to easily cross the gastrointestinal tract and the blood-brain barrier by membrane permeability assays. 59 Baicalein has demonstrated neuroprotective properties to dopaminergic neurons implicated in the pathogenesis of Parkinson’s disease. Animal subjects given MPTP (a dopamine neurotoxin) in combination with Baicalein demonstrated decreased neuronal damage and microglia activation. 60 61 62 63 Baicalein has been reported to protect cortical neurons from beta-amyloid, the protein involved in Alzheimer’s disease. 64 It has demonstrated to ameliorate inflammatory processes of diabetic retinopathy and have inhibitory activity against neuron loss in diabetic retinas. 65 Baicalein has been found to protect neurons from decreased blood flow to the brain. 66 67 Traumatic brain injury triggers a complex series of inflammatory responses that contribute to secondary damage. Research has found that post-injury treatment with baicalein improved functional outcomes and reduced pro-inflammatory activity in traumatic brain injury. 68
 
Resveratrol (flavonoid)
Resveratrol, a flavonoid found in grapes and wine, has been reported to reduce the activation of microglia in numerous studies. Activated microglia produce excessive nitric oxide, which leads to neuronal inflammation. Resveratrol has demonstrated nitric oxide attenuating properties on microglia cells. 69 70 Resveratrol has potent antioxidant effects on oxidative stress activity derived from microglia cell activation. 71 72 Resveratrol reduces activated microglia cell activity and may reduce neuroinflammation. 73 74 Resveratrol has demonstrated the ability to protect against microglia-dependant amyloid-beta toxicity through inhibiting NF-kappaB signaling and may provide a novel compound to be considered for Alzheimer’s disease. 75 Research on resveratrol has found it inhibits LPS-induced nitric oxide and TNF-alpha production in microglia by blocking phosphorylation, and is suggested as potential support compound for neurodegenerative conditions. 76 77
 
Rutin (flavonoid)
Rutin, a citrus flavonoid found in plants, acts as a powerful antioxidant. It attaches to the iron ion Fe2 +, preventing it from binding to hydrogen peroxide and allowing it to become a free radical. Rutin has demonstrated the ability to quench lipid peroxidation. 78 It has demonstrated the ability to modulate microglia inflammatory mediators TNF-alpha and nitric oxide. 79 It has been found to protect against toxicant-induced hippocampal injury by suppression of microglia activation of inflammatory cytokines. 80
 
Catechins (found in teas)
Catechins are polyphenolic antioxidant plant metabolites abundant in various tea leaves. They have been shown to protect microglia cells and neurons from DNA damage by oxidative stress by increasing their expression of DNA repair by the enzyme poly( ADP-ribose) polymerase and by translocation of NF-kappaB. 81 82 Catechins have been reported to possess divalent metal chelating, antioxidant, and anti-inflammatory activities, to penetrate the brain barrier, and to protect neuronal death in a wide array of cellular and animal models of neurological disorders. They appear to have both an iron chelating and antioxidant effect. 83 84 One study demonstrated catechin is a potent inhibitor of microglia activation and thus is a useful candidate for alleviating microglia-mediated neuronal injury. 85
 
Curcumin
Curcumin are antioxidant compounds found in the Indian curry spice of turmeric that have been found to modulate microglia neuroinflammation. Curcumin has demonstrated the ability to protect dopaminergic neurons against LPS-induced neurotoxicity in animal neuronal/ glia culture. 86 Curcumin has been found to have neuroprotective effects by blocking the production of pro-inflammatory and cytotoxic mediators such as nitric oxide, TNF-alpha, IL-1 alpha, IL-6, and NF-kappaB by activated microglia. 87 88 89 90 91 Curcumin has been found to inhibit amyloid peptide-induced chemokine gene expression and may represent a potential therapeutic aid to ameliorate the inflammation and progression of Alzheimer’s disease.
Increase your intake of curry, a staple in India, where there is a low incidence of Alzheimer’s. Turmeric, the spice that gives curry its color, is an excellent source of curcumin, one of the most powerful, natural anti-inflammatories (and antioxidants). Animal studies show that curcumin lowers levels of inflammation in the brain and reduces beta-amyloid plaque by up to 50 percent. A human study also revealed that people who ate curry had significantly better scores on tests of cognitive function than those who never ate it. If you can’t tolerate the taste of curry, you can also supplement with curcumin. The suggested daily dose is 1,000–2,000 mg of regular curcumin or 500–1,000 mg of curcumin phytosome.
 
[Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? (pp. 214-215). Elephant Press. Kindle Edition. ]
 
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The following three show significant effects in the schizophrenia study below:
 
Aspirin
 
Can cause stomach to bleed with chronic usage. Finding a low effective dose can avoid this.
 

The ability of ASA to increase anti-inflammatory LXA₄ and 15-epi-LXA₄ and reduce pro-inflammatory PGE₂ and TXB₂ suggests considering aspirin further for treating clinical neuroinflammation.

 
[]http://www.ncbi.nlm.nih.gov/pubmed/20981485]
 
Estrogens
 
 

Estrogens regulate neuroinflammatory genes via estrogen receptors α and β in the frontal cortex of middle-aged female rats.
Abstract

BACKGROUND:
Estrogens exert anti-inflammatory and neuroprotective effects in the brain mainly via estrogen receptors α (ERα) and β (ERβ). These receptors are members of the nuclear receptor superfamily of ligand-dependent transcription factors. This study was aimed at the elucidation of the effects of ERα and ERβ agonists on the expression of neuroinflammatory genes in the frontal cortex of aging female rats.
METHODS:
To identify estrogen-responsive immunity/inflammation genes, we treated middle-aged, ovariectomized rats with 17β-estradiol (E2), ERα agonist 16α-lactone-estradiol (16α-LE2) and ERβ agonist diarylpropionitrile (DPN), or vehicle by Alzet minipump delivery for 29 days. Then we compared the transcriptomes of the frontal cortex of estrogen-deprived versus ER agonist-treated animals using Affymetrix Rat230 2.0 expression arrays and TaqMan-based quantitative real-time PCR. Microarray and PCR data were evaluated by using Bioconductor packages and the RealTime StatMiner software, respectively.
RESULTS:
Microarray analysis revealed the transcriptional regulation of 21 immunity/inflammation genes by 16α-LE2. The subsequent comparative real-time PCR study analyzed the isotype specific effects of ER agonists on neuroinflammatory genes of primarily glial origin. E2 regulated the expression of sixteen genes, including down-regulation of complement C3 and C4b, Ccl2, Tgfb1, macrophage expressed gene Mpeg1, RT1-Aw2, Cx3cr1, Fcgr2b, Cd11b, Tlr4 and Tlr9, and up-regulation of defensin Np4 and RatNP-3b, IgG-2a, Il6 and ER gene Esr1. Similar to E2, both 16α-LE2 and DPN evoked up-regulation of defensins, IgG-2a and Il6, and down-regulation of C3 and its receptor Cd11b, Ccl2, RT1-Aw2 and Fcgr2b.
CONCLUSIONS:
These findings provide evidence that E2, 16α-LE2 and DPN modulate the expression of neuroinflammatory genes in the frontal cortex of middle-aged female rats via both ERα and ERβ. We propose that ERβ is a promising target to suppress regulatory functions of glial cells in the E2-deprived female brain and in various neuroinflammatory diseases.

 
[]http://www.ncbi.nlm.nih.gov/pubmed/21774811]
 
NAC
 

There is an expanding field of research investigating the benefits of alternatives to current pharmacological therapies in psychiatry. [/size]N-acetylcysteine (NAC) is emerging as a useful agent in the treatment of psychiatric disorders. Like many therapies, the clinical origins of NAC are far removed from its current use in psychiatry. Whereas the mechanisms of NAC are only beginning to be understood, it is likely that NAC is exerting benefits beyond being a precursor to the antioxidant, glutathione, modulating glutamatergic, neurotropic and inflammatory pathways. This review outlines the current literature regarding the use of NAC in disorders including addiction, compulsive and grooming disorders, schizophrenia and bipolar disorder. [/size]N-acetylcysteine has shown promising results in populations with these disorders, including those in whom treatment efficacy has previously been limited. The therapeutic potential of this acetylated amino acid is beginning to emerge in the field of psychiatric research.[/size]

 
[]http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3044191/]
 
Astaxanthin
is now thought to be the most powerful antioxidant found in nature. 

  • Astaxanthin is by far the most powerful carotenoid antioxidant when it comes to free radical scavenging: astaxanthin is 65 times more powerful than vitamin C, 54 times more powerful than beta-carotene, and 14 times more powerful than vitamin E.
  • Astaxanthin is far more effective than other carotenoids at "singlet oxygen quenching," which is a particular type of oxidation. The damaging effects of sunlight and various organic materials are caused by this less-stable form of oxygen. Astaxanthin is 550 times more powerful than vitamin E and 11 times more powerful than beta-carotene at neutralizing singlet oxygen.
  • Astaxanthin crosses the blood-brain barrier AND the blood-retinal barrier, which brings antioxidant and anti-inflammatory protection to your eyes, brain and central nervous system and reducing your risk for cataracts, macular degeneration, blindness, dementia and Alzheimer's disease.
  • Astaxanthin is soluble in lipids, so it incorporates into cell membranes.
  • It's a potent UVB absorber and reduces DNA damage.
  • It's a very potent natural anti-inflammatory.

 

Efficacy of Anti-inflammatory Agents to Improve Symptoms in Patients With Schizophrenia: An Update
Abstract
Background: The inflammatory hypothesis of schizophrenia is not new, but recently it has regained interest because more data suggest a role of the immune system in the pathogenesis of schizophrenia. If increased inflammation of the brain contributes to the symptoms of schizophrenia, reduction of the inflammatory status could improve the clinical picture. Lately, several trials have been conducted investigating the potential of anti-inflammatory agents to improve symptoms of schizophrenia. This study provides an update regarding the efficacy of anti-inflammatory agents on schizophrenic symptoms in clinical studies performed so far.Methods: An electronic search was performed using PubMed, Embase, the National Institutes of Health web site http://www.clinicaltrials.gov, Cochrane Schizophrenia Group entries in PsiTri, and the Cochrane Database of Systematic Reviews. Only randomized, double-blind, placebo-controlled studies that investigated clinical outcome were included.Results: Our search yielded 26 double-blind randomized controlled trials that provided information on the efficacy on symptom severity of the following components: aspirin, celecoxib, davunetide, fatty acids such as eicosapentaenoic acids and docosahexaenoic acids, estrogens, minocycline, and N-acetylcysteine (NAC). Of these components, aspirin (mean weighted effect size [ES]: 0.3, n = 270, 95% CI: 0.06–0.537, I2 = 0), estrogens (ES: 0.51, n = 262, 95% CI: 0.043–0.972, I2 = 69%), and NAC (ES: 0.45, n = 140, 95% CI: 0.112–0.779) showed significant effects. Celecoxib, minocycline, davunetide, and fatty acids showed no significant effect. Conclusion: The results of aspirin addition to antipsychotic treatment seem promising, as does the addition of NAC and estrogens. These 3 agents are all very broadly active substances, and it has to be investigated if the beneficial effects on symptom severity are indeed mediated by their anti-inflammatory aspects.

 

 

Sources:

http://www.drwhitaker.com/protect-your-brain-with-natural-anti-inflammatories

http://www.ncbi.nlm.nih.gov/pubmed/21143138
http://www.dana.org/News/Details.aspx?id=43258
http://articles.mercola.com/sites/articles/archive/2011/07/12/astaxanthin-the-antiinflammatory-nutrient.aspx

Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? Elephant Press.

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  • 11 months later...

I take NAC as recommended by some and I try to use 1-2 grams of curcumin and some black pepper in one dish a day (as black pepper potentiates curcumin's antioxidant effect x1000 apparently). It could be scrumbled egg or mashed avocado with garlic, salt and lemon.

I hope this is enough of antioxidants daily :)

 

I wonder does anybody here has any good antioxidant daily stock?

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